Cardiomyocyte necrosis mainly contributes to heart failure, while the underlying mechanism is not fully explained.35 H19, which contains three potential miR‐103/107 binding sites, prevented cardiomyocyte necrosis via inhibiting the level of miR‐103/107 and its target Fas‐associated protein with death domain (FADD) in response to H2O2 treatment, while these effects were offset by silencing H19.36 Another lncRNA, named necrosis‐related factor (NRF), was closely related to necrotic death of cardiomyocytes by acting as an endogenous RNA sponge that interacted with miR‐873 in the cytoplasm. This evidence concerns the gene H19 and heart failure.